Oncological Emergencies Flashcards
What is tumour lysis syndrome?
Rapid destruction of cancer cells after chemo or spontaneously which leads to intra cellular contents being released into the blood stream.
What does tumour lysis syndrome lead to.
An elevation in serum uric acid, K+, phosphate, and a reduction in serum Ca2+ levels.
Which patients are at a particular risk of having tumour lysis syndrome?
. High tumour burden . Rapidly proliferating tumour . Haematological disease . Bulky disease . Pre existing renal impairment . Hypovolaemia . Diuretic use pre treatment . High levels of LDH/ uric acid in the serum pre treatment
What do you need to diagnose tumour lysis syndrome?
1 clinical feature + 2 lab features….
Clinical features... . An increased serum creatinine . Cardiac arrythmia . Seizure . Sudden death
2 lab features... . Increased uric acid . Increased K+ . Increased phosphate . Decreased Ca2+
How can you help prevent tumour lysis syndrome?
Hydration is key before and after chemo to stop uric acid from accumulating
Patients at risk of TLS should be given allopurinol or Rasburicase
(These are medications that help clear uric acid from the blood)
How does rasburicase work?
Converts uric acid to allantoin which is much more water soluble and therefore more gets excreted in the kidney.
How does allopurinol work?
Xanthine oxidase inhibitor which lowers the uric acid levels
Should you ever give rasburicase and allopurinol together?
Never, allopurinol reduces the affect of rasburicase.
How can you lower uric acid levels if rasburicase and allopurinol don’t work, if refractory or severely raised?
Dialysis can be used
What is the risk of tumour lysis syndrome?
AKI and permanent renal damage
How do you manage tumour lysis syndrome?
Fluids!!!!
IV rasburicase +/- dialysis (for severe renal impairement)
10ml IV calcium gluconate 10% for symptomatic hypocalcaemia
Insulin and dextrose
What is neutropenic sepsis?
A severe widespread response to an infection which is greatly exaggerated due to the low levels of neutrophils in a patient undergoing chemo.
When does neutropenic sepsis usually occur?
5-14 days after chemo when neutrophils are at the lowest.
What are the usual causative organisms of neutropenic sepsis?
Usually endogenous flora- staph aureus
Although a lot of the time no causative organisms are found.
What patients are at risk of neutropenic sepsis?
Inpatients
Those with severe/prolonged neutropaenia
Those with significant co morbidities like COPD/ diabetes
Those with central lines/mucosal disruption
How is neutropenic sepsis diagnosed?
Bloods- FBC, U and Es, LFTs, blood cultures, CRP, lactate
Sepsis 6
CXR
Urine, stool, sputum if clinically indicated
Central and peripheral line swabs
Swabs of catheters/ indwelling lines
When is a diagnosis of neutropenic sepsis made?
Neutrophil count <0.5x10^9
They have been receiving systemic anticancer therapy
They have a temp >38 or other signs of sepsis
How do you manage neutropenic sepsis?
Broad spec abx with IV tazocin or meropenem
Fluid resuscitation and fluid balance
G-CSF can be given to boost the patients immune system (artificial neutrophils)
How can you prevent neutropenic sepsis from occuring?
Prophylactic abx- fluoroquinolone
Patients should carry around a yellow alert card
Patients should be made aware of warning signs
24 hour contact number for help if they notice signs of infection
Beyond what level is spinal cord compression classed as cauda equina?
Below the level of L2
What is the NICE definition of neutropenic sepsis?
Patient undergoing systemic anti cancer treatment (SACT)
Temp >38
Neutrophil count <0.5 x 10^9 per litre
When does neutropaenia typically occur after chemo?
Typically occurs day 10-14
What are the signs and symptoms of neutropenic sepsis?
Fever
Symptoms related to a specific system- cough, SOB
Drowsy
Confused
Signs Febrile Tachy >90 Hypotension <90 systolic- needs urgent attention RR >20 Impaired MMSE Signs of infection
What are the most common pathogens which cause neutropaenic sepsis?
80% arise from endogenous flora (due to disruption of mucosal lining)
Increasing frequency of gram +ve cocci; indwelling plastic catheters promote colonisation
Most frequent isolates= staph aureus, staph epidermidis, enterococcus and streptococcus
MRSA and VRE are increasingly prevalent
Source identified in approximately 30% of patients
What investigations are done for someone with neutropaenic sepsis?
Blood tests: FBC (with differential) U and Es LFTS Lactate CRP ABG
Cultures
Blood- central and peripheral
Urine
sputum
Swabs
Lines
Wounds
Imaging
Directed clinically
CXR, AXR, CT/MRI
What is the differential diagnosis for neutropaenic sepsis?
Malignant related fever
PE
Chemo related fever
What is the management of neutropaenic sepsis?
Dont wait for the FBC Empiric IV broad spec within the hour (meropenem or Fluid rescucitation Consider catheterisation Involve senior members of rhe ream Consider the need for escalation of care
What can be considered in patients who are profoundly septic/neutropenic where you have already done the above management?
GCSF (granulocyte colony stimulating factor)
How can you avoid neutropaenic sepsis?
Patient education- how and when to contact 24 hour specialist oncology advice/ seek emergency care
Antibiotic prophylaxis (versus increased antibiotic resistance)
Dose reduction (palliative chemo), prophylactic GCSF (curative/ adjuvant) should be Considered for future chemo cycles
All patients should be issues with an alert card with 24 hour contact numbers
What cancers are most likely to metastasise to the spine?
Breast, lung, prostate
At what level does cauda equina occur?
Below L2, cauda equina is the compression of peripheral nerves not the spinal cord
What is the pathophysiology behind metastatic spinal cord compression?
Usually caused by collapse or compression of a vertebral body that contains metastatic disease (arterial seeding)
10% by direct tumour (paraspinal mass) extension into the vertebral column
Compression of the cord initially causes oedema, venous congestion and demyelination which are reversible
Prolonged compression leads to vascular injury, cord necrosis and permanent damage
How does MSCC present?
> 90% have back pain
Back pain is frequently the first symptom and prolonged; often precedes other symptoms by 2-3/12
Spinal or radicular pain (8/10)
Exacerbated by straight leg raising, coughing, sneezing, straining
> 75% have limb weakness
50% have sensory level (not cauda equina)
40% have bladder and anal sphincter dysfunction
Diminishing performance status/generally unwell
What presentation would someone have on examination with spinal cord compression due to mets?
Acute onset of flaccid paralysis
Progressing over time.,,
Spasticity (increased tone, clonus, hyperreflexia in limbs) below the level of metastatic spinal cord compression
Plantar reflexes would be up going (but not with cauda equina)
Sensory loss with a well defined dermatonal level
Palpable bladder (urinary retention)
What should you do if you suspect MCSS?
MRI within 24 hours Admit Bed rest with log rolling Dexamethasone 16mg + PPI Adequate analgesia Treatment within 24 hours of diagnosis
What is the treatment of MSCC?
The treatment of choice is surgery if fit and good prognosis (>3/12)
Multiple myeloma, lymphoma, breast, prostate, renal cancers
Good motor function at presentation, good performance status, limited comorbidity, single level spinal disease, absence of visceral mets, long interval from primary diagnosis, also for biopsy or stabilisation
What does the surgery do?
Relieves compression
Removes tumour and stabilises spine
What other options other than surgery do you have for MCSCC?
Balloon kyphoplasty
Radiotherapy (this is what is used for the majority with extensive disease and poor physiological reserve), it should be delivered within 24 hours of confirmation
How does radiotherapy work for MCSCC?
It relieves compression of the spine and nerve roots by causing cell death in the rapidly dividing tumour tissue.
What are the supportive care options for MCSCC?
Good nursing care, Analgesia Laxatives Bladder care Monitor BMs VTE prophylaxis Physiotherapy Occupational therapy Urgent chemo for sensitive tumours- lymphoma, teratoma, SCLC
What is the median survival of people with MSCC?
Those who do not recover their mobility: 1-3/12
If they can walk: 5-8/12
Patients with myeloma/lymphoma have an even longer prognosis
What is the normal calcium range?
2.2-2.6mmol/L (corrected)
What is hypercalcaemia most common in?
Most common in squamous cell cancers (lung, H and N, kidney, cervix).
What is hypercalcaemia usually caused by in terms of cancerz?
Generally due to a paraneoplastic phenomenon (tumour secretion PTH related peptide)
This leads to…
Increased bone resorption and renal reabsorption
Unrelated to the extent of bone mets
(80%)
Other causes…
Osteolytic metastases with local release of cytokines (20%), causes increased bone resorption and calcium release from bone (local bone destruction)
Tumour production of 1,25 dihydroxy vitamin D (lymphoma) leads to increased intestinal calcium absorption and bone resorption
What are the symptoms of hypercalcaemia in the cancer patient?
Often non specific; the severity relates to the rate of increase Nauseated Anorexia Thirsty Polydipsia and polyuria Fatigue and weakness Constipated Confused Poor concentration Drowsy Severe N&V, ileus, delirium, coma and death
How do you treat hyprcalcaemia?
FLUIDS!! Rehydration is so important, there should be at least 24 hours of normal saline.
Bisphosphonates
60-90mg pamidronate IV or IV zolendronic acid 4mg
Bisphosphonates can cause renal failure therefore you should make sure the patient is properly rehydrated first
Bisphosphonates can take up to a week to work
How do you treat hypercalcaemia that is refractory to zoledronic acid/ bisphosphonates are contraindicated in?
Denosumab
What is tumour lysis syndrome?
Massive tumour cell lysis which leads to the release of large amounts of K+, phosphate and uric acid into the systemic circulation Leads to... Hyperuricaemia Hyperkalaemia Hyperphosphataemia AKI Hypocalcaemia
What are the susceptible tumour types for tumour lysis syndrome?
The risk is greatest for haematological malignancies
Bulky chemo responsive tumours
Most common with high grade lymphomas and leukaemias
It is generally following the initiation of cytotoxic therapy
What are the patient specific risk factors for tumour lysis syndrome?
Pre existing renal dysfunction/nephropathy
Pre treatment hyperuricaemia
Hypovolaemia (pre treatment diuretic use)
Pre treatment high LDH
Urinary tract obstruction from tumour
What is the presentation of tumour lysis syndrome?
This is normally 3-7 day post chemo Nausea and vomiting Diarrhoea Anorexia Lethargy Haematuria -> oliguria -> anuric Heart failure Cardiac arrythmias/arrest (peaked T waves, QTc derangement) Primary presentation of malignancy= ‘spontaneous tumour lysis’
How do you prevent/treat tumour lysis syndrome?
Pre hydration and vigorous hydration throughout treatment
Monitoring of electrolytes and fluid balance
Allopurinol
Rasburicase
What is SVCO?
Obstruction of blood flow through the SVC
Compression or occlusion of SVC
90% are usually extrinsic compression- intrathoracic primary, lung cancer (80%), mesothelioma
Can occasionally get a benign obstruction- thrombus
Uncommon causes= post RT fibrosis, TB
What are the signs and symptoms of SVC obstruction?
Breathlessness (50%) Swelling of the face and neck (40%) Trunk and arm swelling (40%) Sensation of choking A feeling of fullness in the head Headache Lethargy Chest pain Cough dysphagia Cognitive dysfunction Hallucinations Seizures Stridor Coma
How do you investigate SVCO?
CT with contrast
What is the treatment of SVCO?
Steroids (frequently prescribed, however there is no evidence to support their use)
Stent: if not radio or chemo sensitive
95% desponse rate
Rapid relief of symptoms, but doesnt actually treat the cause
Chemo used for SCLC, lymphoma, teratoma (response rate >70%)
Radiotherapy- used for other malignant causes
